CONGESTIVE HEART FAILURE

Heart failure (HF) is a clinical syndrome resulting from structural or functional cardiac
disorders that impair the ability of the ventricles to fill or eject blood (Yancy, Jessup, Bozkurt,
et al., 2013). In the past, HF was often referred to as congestive heart failure (CHF),
because many patients experience pulmonary or peripheral congestion with edema.
Currently, HF is recognized as a clinical syndrome characterized by signs and symptoms of
fluid overload or inadequate tissue perfusion. Fluid overload and decreased tissue perfusion
result when the heart cannot generate cardiac output (CO) sufficient to meet the body’s
demands for oxygen and nutrients. The term heart failure indicates myocardial disease in
which impaired contraction of the heart (systolic dysfunction) or filling of the heart (diastolic
dysfunction) may cause pulmonary or systemic congestion. Some cases of HF are
reversible, depending on the cause. Most often, HF is a chronic, progressive condition that is
managed with lifestyle changes and medications to prevent episodes of acute
decompensated heart failure. These episodes are characterized by increased symptoms,
decreased CO, and low perfusion. These episodes are also associated with increased
hospitalizations, increased health care costs, and decreased quality of life.

Myocardial dysfunction and HF can be caused by a number of conditions, including

coronary artery disease, hypertension, cardiomyopathy, valvular disorders, and renal
dysfunction with volume overload. Patients with diabetes are also at high risk for HF.
Atherosclerosis of the coronary arteries is a primary cause of HF, and coronary artery
disease is found in the majority of patients with HF. Ischemia causes myocardial dysfunction
because it deprives heart cells of oxygen and causes cellular damage. MI causes focal heart
muscle necrosis, the death of myocardial cells, and a loss of contractility; the extent of the
infarction correlates with the severity of HF. Revascularization of the coronary artery by a
percutaneous coronary intervention (PCI) or by coronary artery bypass surgery (coronary
artery bypass graft [CABG]) may improve myocardial oxygenation and ventricular function
and prevent more extensive myocardial necrosis that can lead to HF. Systemic or pulmonary
hypertension increases afterload (resistance to ejection), which increases cardiac workload
and leads to hypertrophy of myocardial muscle fibers. This can be considered a
compensatory mechanism because it initially increases contractility. However, sustained
hypertension eventually leads to changes that impair the heart’s ability to fill properly during
diastole, and the hypertrophied ventricles may dilate and fail. Cardiomyopathy is a disease
of the myocardium. The various types of cardiomyopathy lead to HF and dysrhythmias.
Dilated cardiomyopathy, the most common type of cardiomyopathy, causes diffuse myocyte
necrosis and fibrosis, and commonly leads to progressive HF. Dilated cardiomyopathy can
be idiopathic (unknown cause), or it can result from an inflammatory process, such as
myocarditis, or from a cytotoxic agent, such as alcohol or certain antineoplastic drugs.
Hypertrophic cardiomyopathy is an autosomal dominant disease which leads to severe
ventricular hypertrophy and poor diastolic filling (diastolic failure). Usually, HF due to
cardiomyopathy is chronic and progressive. However, cardiomyopathy and HF may resolve
following removal of the causative agent (e.g., cessation of alcohol ingestion). Valvular heart
disease is also a cause of HF. The valves ensure that blood flows in one direction. With
valvular dysfunction, it becomes increasingly difficult for blood to move forward, increasing
pressure within the heart and increasing cardiac workload, leading to HF. See Chapter 28 for
discussion of the effects of valvular heart disease. Several systemic conditions, including
progressive renal failure, contribute to the development and severity of HF. More than 40%
of patients with chronic HF have impaired renal function. The term cardiorenal syndrome
describes how dysfunction in one of these systems leads to dysfunction in the other,
resulting in increased morbidity and mortality. In addition, cardiac dysrhythmias such as
atrial fibrillation may either cause or result from HF; in both instances, the altered electrical
stimulation impairs myocardial contraction and decreases the overall efficiency of myocardial
function. Other factors, such as hypoxia, acidosis, and electrolyte abnormalities, can worsen
myocardial function.

Regardless of the etiology, the pathophysiology of HF results in similar changes and

clinical manifestations. Significant myocardial dysfunction usually occurs before the patient
experiences signs and symptoms of HF such as shortness of breath, edema, or fatigue. As
HF develops, the body activates neurohormonal compensatory mechanisms. These
mechanisms represent the body’s attempt to cope with the HF and are responsible for the
signs and symptoms that develop. Understanding these mechanisms is important because
the treatment for HF is aimed at correcting them and relieving symptoms. Systolic HF results
in decreased blood ejected from the ventricle. The decreased blood flow is sensed by
baroreceptors in the aortic and carotid bodies. The sympathetic nervous system is then
stimulated to release epinephrine and norepinephrine. The purpose of this initial response is
to increase heart rate and contractility and support the failing myocardium, but the continued
response has multiple negative effects. Sympathetic stimulation causes vasoconstriction in
the skin, gastrointestinal tract, and kidneys. A decrease in renal perfusion due to low CO and
vasoconstriction then causes the release of renin by the kidneys. Renin converts the plasma
protein angiotensinogen to angiotensin I, which then circulates to the lungs. Angiotensin-
converting enzyme (ACE) in the lumen of pulmonary blood vessels converts angiotensin I to
angiotensin II, a potent vasoconstrictor, which then increases the blood pressure and
afterload. Angiotensin II also stimulates the release of aldosterone from the adrenal cortex,
resulting in sodium and fluid retention by the renal tubules and an increase in blood volume.
These mechanisms lead to the fluid volume overload commonly seen in HF. Angiotensin,
aldosterone, and other neurohormones (e.g., endothelin) lead to an increase in preload and
afterload, which increases stress on the ventricular wall, causing an increase in cardiac
workload. A counter-regulatory mechanism is attempted through the release of natriuretic
peptides. Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP; brain type) are
released from the overdistended cardiac chambers. These substances promote vasodilation
and diuresis. However, their effect is usually not strong enough to overcome the negative
effects of the other mechanisms. As the heart’s workload increases, contractility of the
myocardial muscle fibers decreases. Decreased contractility results in an increase in end-
diastolic blood volume in the ventricle, stretching the myocardial muscle fibers and
increasing the size of the ventricle (ventricular dilation). One way the heart compensates for
the increased workload is to increase the thickness of the heart muscle (ventricular
hypertrophy). However, hypertrophy results in abnormal changes in structure and function of
myocardial cells, a process known as ventricular remodeling. Under the influence of
neurohormones (e.g., angiotensin II), enlarged myocardial cells become dysfunctional and
die early (a process called apoptosis), leaving the other normal myocardial cells struggling to
maintain CO. As cardiac cells die and the heart muscle becomes fibrotic, diastolic HF can
develop, leading to further dysfunction. A stiff ventricle resists filling, and less blood in the
ventricles causes a further decrease in CO. All of these compensatory mechanisms of HF
have been referred to as the “vicious cycle of HF” because low CO leads to multiple
mechanisms that make the heart work harder, worsening the HF.
 Many clinical manifestations are associated with HF. These signs and symptoms are
related to congestion and poor perfusion. The signs and symptoms of HF can also be related
to the ventricle that is most affected. Left-sided heart failure (left ventricular failure) causes
different manifestations than right-sided heart failure (right ventricular failure). In chronic HF,
patients may have signs and symptoms of both left and right ventricular failure. Left-Sided
Heart Failure. Pulmonary congestion occurs when the left ventricle cannot effectively pump
blood out of the ventricle into the aorta and the systemic circulation. The increased left
ventricular end-diastolic blood volume increases the left ventricular end-diastolic pressure,
which decreases blood flow from the left atrium into the left ventricle during diastole. The
blood volume and pressure build up in the left atrium, decreasing flow through the pulmonary
veins into the left atrium. Pulmonary venous blood volume and pressure increase in the
lungs, forcing fluid from the pulmonary capillaries into the pulmonary tissues and alveoli,
causing pulmonary interstitial edema and impaired gas exchange. The clinical
manifestations of pulmonary congestion include dyspnea, cough, pulmonary crackles, and
low oxygen saturation levels. An extra heart sound, the S3, or “ventricular gallop,” may be
detected on auscultation. It is caused by abnormal ventricular filling (Pinkerman et al., 2013).
Dyspnea, or shortness of breath, may be precipitated by minimal to moderate activity
(dyspnea on exertion [DOE]); dyspnea also can occur at rest. The patient may report
orthopnea, difficulty breathing when lying flat. Patients with orthopnea may use pillows to
prop themselves up in bed, or they may sit in a chair and even sleep sitting up. Some
patients have sudden attacks of dyspnea at night, a condition known as paroxysmal
nocturnal dyspnea (PND). Fluid that accumulates in the dependent extremities during the
day may be reabsorbed into the circulating blood volume when the patient lies down.
Because the impaired left ventricle cannot eject the increased circulating blood volume, the
pressure in the pulmonary circulation increases, shifting fluid into the alveoli. The fluid filled
alveoli cannot exchange oxygen and carbon dioxide. Without sufficient oxygen, the patient
experiences dyspnea and has difficulty sleeping. The cough associated with left ventricular
failure is initially dry and nonproductive. Most often, patients complain of a dry hacking
cough that may be mislabeled as asthma or chronic obstructive pulmonary disease (COPD).
The cough may become moist over time. Large quantities of frothy sputum, which is
sometimes pink or tan (blood tinged), may be produced, indicating acute decompensated HF
with pulmonary edema. Adventitious breath sounds may be heard in various areas of the
lungs. Usually, bibasilar crackles that do not clear with coughing are detected in the early
phase of left ventricular failure. As the failure worsens and pulmonary congestion increases,
crackles may be auscultated throughout the lung fields. At this point, oxygen saturation may
decrease. In addition to pulmonary manifestations, the amount of blood ejected from the left
ventricle decreases and can lead to inadequate tissue perfusion. The diminished CO has
widespread manifestations because not enough blood reaches all of the tissues and organs
(low perfusion) to provide the necessary oxygen. The decrease in stroke volume (SV) can
also stimulate the sympathetic nervous system to release catecholamines, which further
impedes perfusion to many organs, including the kidneys. As reduced CO and
catecholamines decrease blood flow to the kidneys, urine output drops (oliguria). Renal
perfusion pressure falls, and the renin– angiotensin–aldosterone system is stimulated to
increase blood pressure and intravascular volume. However, when the patient is sleeping,
the cardiac workload is decreased, improving renal perfusion, which in some patients leads
to frequent urination at night (nocturia). As HF progresses, decreased output from the left
ventricle may cause other symptoms. Decreased gastrointestinal perfusion causes altered
digestion. Decreased brain perfusion causes dizziness, lightheadedness, confusion,
restlessness, and anxiety due to decreased oxygenation and blood flow. As anxiety
increases, so does dyspnea, increasing anxiety and creating a vicious cycle. Stimulation of
the sympathetic system also causes the peripheral blood vessels to constrict, so the skin
appears pale or ashen and feels cool and clammy. A decrease in SV causes the
sympathetic nervous system to increase the heart rate (tachycardia), often causing the
patient to complain of palpitations. The peripheral pulses become weak. Without adequate
CO, the body cannot respond to increased energy demands, and the patient becomes easily
fatigued and has decreased activity tolerance. Fatigue also results from the increased
energy expended in breathing and the insomnia that results from respiratory distress,
coughing, and nocturia. Right-Sided Heart Failure. When the right ventricle fails, congestion
in the peripheral tissues and the viscera predominates. This occurs because the right side of
the heart cannot eject blood effectively and cannot accommodate all of the blood that
normally returns to it from the venous circulation. Increased venous pressure leads to jugular
venous distention (JVD) and increased capillary hydrostatic pressure throughout the venous
system. Systemic clinical manifestations include edema of the lower extremities (dependent
edema), hepatomegaly (enlargement of the liver), ascites (accumulation of fluid in the
peritoneal cavity), and weight gain due to retention of fluid. Edema usually affects the feet
and ankles and worsens when the patient stands or sits for a long period. The edema may
decrease when the patient elevates the legs. Edema can gradually progress up the legs and
thighs and eventually into the external genitalia and lower trunk. Ascites is evidenced by
increased abdominal girth and may accompany lower body edema or may be the only
edema present. Sacral edema is common in patients who are on bed rest, because the
sacral area is dependent. Pitting edema, in which indentations in the skin remain after even
slight compression with the fingertips, is generally obvious after retention of at least 4.5 kg
(10 lb) of fluid (4.5 L). Hepatomegaly and tenderness in the right upper quadrant of the
abdomen result from venous engorgement of the liver. The increased pressure may interfere
with the liver’s ability to function (secondary liver dysfunction). As hepatic dysfunction
progresses, increased pressure within the portal vessels may force fluid into the abdominal
cavity, causing ascites. Ascites may increase pressure on the stomach and intestines and
cause gastrointestinal distress. Hepatomegaly may also increase pressure on the
diaphragm, causing respiratory distress. Anorexia (loss of appetite), nausea, or abdominal
pain may result from the venous engorgement and venous stasis within the abdominal
organs. The generalized weakness that accompanies right-sided HF results from reduced
CO and impaired circulation.

HF may go undetected until the patient presents with signs and symptoms of
pulmonary and peripheral edema. Some of the physical signs that suggest HF may also
occur with other diseases, such as kidney injury and COPD; therefore, diagnostic testing is
essential to confirm a diagnosis of HF. Assessment of ventricular function is an essential
part of the initial diagnostic workup. An echocardiogram is usually performed to determine
the EF, identify anatomic features such as structural abnormalities and valve malfunction,
and confirm the diagnosis of HF. This information may also be obtained noninvasively by
radionuclide ventriculography or invasively by ventriculography as part of a cardiac
catheterization procedure. Differential identification of systolic and diastolic HF is important,
as treatment differs (Pinkerman et al., 2013). A chest x-ray and a 12-lead electrocardiogram
(ECG) are obtained to assist in the diagnosis. Laboratory studies usually performed during
the initial workup include serum electrolytes, blood urea nitrogen (BUN), creatinine, liver
function tests, thyroid-stimulating hormone, complete blood count (CBC), BNP, and routine
urinalysis. The BNP level is a key diagnostic indicator of HF; high levels are a sign of high
cardiac filling pressure and can aid in both the diagnosis and management of HF. The
results of these laboratory studies assist in determining the underlying cause and can also
be used to establish a baseline to assess effects of treatment. Cardiac stress testing or
cardiac catheterization may be performed to determine whether coronary artery disease and
cardiac ischemia are causing the HF.

Medical Management. The goals of management of HF are to relieve patient

symptoms, to improve functional status and quality of life, and to extend survival. The
prognosis for HF patients has improved with the use of evidence-based protocols for patient
management. Specific interventions are based on the stage of HF. The objectives of
guideline-directed patient management include the following: improvement of cardiac
function with optimal pharmacologic management, reduction of symptoms and improvement
of functional status, stabilization of patient condition and lowering of the risk of
hospitalization, delay of the progression of HF and extension of life expectancy, promotion of
a lifestyle conducive to cardiac health, treatment options vary according to the severity of the
patient’s condition and may include oral and intravenous (IV) medications, major lifestyle
changes, supplemental oxygen, and surgical interventions including implantation of cardiac
devices and cardiac transplantation. Managing the patient with HF begins with providing
comprehensive education and counseling to the patient and family. The patient and family
must understand the nature of HF and the importance of their participation in the treatment
regimen. Lifestyle recommendations include restriction of dietary sodium; avoidance of
smoking, including passive smoke; avoidance of excessive fluid and alcohol intake; weight
reduction when indicated; and regular exercise. The patient must also know how to
recognize signs and symptoms that need to be reported to the primary provider.

Pharmacologic Therapy. Several medications are routinely prescribed for HF,

including ACE inhibitors, beta-blockers, and diuretics. Many of these medications,
particularly ACE inhibitors and beta-blockers, improve symptoms and extend survival.
Others, such as diuretics, improve symptoms but may not affect survival. Target doses for
these medications are identified in the ACC/AHA guidelines, and nurses and physicians
work collaboratively toward achieving effective dosing of these medications (Yancy et al.,
2013).

Angiotensin-Converting Enzyme Inhibitors. ACE inhibitors play a pivotal role in the

management of systolic HF. They have been found to relieve the signs and symptoms of HF
and significantly decrease mortality and morbidity, especially in patients with a left ventricular
EF less than 35%. ACE inhibitors (e.g., lisinopril [Prinivil]) slow the progression of HF,
improve exercise tolerance, and decrease the number of hospitalizations (Yancy et al.,
2013). Available as oral and IV medications, ACE inhibitors promote vasodilation and
diuresis, ultimately decreasing afterload and preload. Vasodilation reduces resistance to left
ventricular ejection of blood, diminishing the heart’s workload and improving ventricular
emptying. ACE inhibitors decrease the secretion of aldosterone, a hormone that causes the
kidneys to retain sodium and water. ACE inhibitors also promote renal excretion of sodium
and fluid (while retaining potassium), thereby reducing left ventricular filling pressure and
decreasing pulmonary congestion. ACE inhibitors may be the first medication prescribed for
patients in mild failure—patients with fatigue or DOE but without signs of fluid overload and
pulmonary congestion. These agents are also recommended for prevention of HF in patients
at risk due to vascular disease and diabetes (Yancy et al., 2013). ACE inhibitors are started
at a low dose that is gradually increased until the optimal dose is achieved and the patient is
hemodynamically stable. The final maintenance dose depends on the patient’s blood
pressure, fluid status, and renal status, as well as the severity of the HF. Patients receiving
ACE inhibitors are monitored for hypotension, hyperkalemia (increased potassium in the
blood), and alterations in renal function, especially if they are also receiving diuretics.
Because ACE inhibitors cause the kidneys to retain potassium, the patient who is also
receiving a diuretic may not need to take oral potassium supplements. However, patients
receiving potassium-sparing diuretics (which do not cause potassium loss with diuresis)
must be carefully monitored for hyperkalemia. ACE inhibitors may be discontinued if the
potassium level remains greater than 5.5 mEq/L or if the serum creatinine rises. Other
adverse effects of ACE inhibitors include a dry, persistent cough that may not respond to
cough suppressants. However, cough can also indicate a worsening of ventricular function
and failure. Rarely, ACE inhibitors can cause an allergic reaction accompanied by
angioedema. If angioedema affects the oropharyngeal area and impairs breathing, the ACE
inhibitor must be stopped immediately and emergency care provided. If the patient cannot
continue taking an ACE inhibitor because of development of cough, an elevated creatinine
level, or hyperkalemia, an angiotensin receptor blocker (ARB) or a combination of
hydralazine and isosorbide dinitrate (Dilatrate) is prescribed.

Angiotensin Receptor Blockers. Although the action of ARBs is different from that of
ACE inhibitors, they (e.g., valsartan [Diovan]) have similar hemodynamic effects and side
effects (Pinkerman et al., 2013). Whereas ACE inhibitors block the conversion of angiotensin
I to angiotensin II, ARBs block the vasoconstricting effects of angiotensin II at the
angiotensin II receptors. ARBs are prescribed for HF patients as an alternative to ACE
inhibitors

Hydralazine and Isosorbide Dinitrate. A combination of hydralazine and isosorbide

dinitrate may be another alternative for patients who cannot take ACE inhibitors. Nitrates
(e.g., isosorbide dinitrate) cause venous dilation, which reduces the amount of blood return
to the heart and lowers preload. Hydralazine lowers systemic vascular resistance and left
ventricular afterload. This combination of medications is also recommended in HF guidelines
and may be more effective for African Americans who do not respond to ACE inhibitors

Beta-Blockers. Beta-blockers are also considered first-line therapy and are routinely
prescribed in addition to ACE inhibitors. These agents block the adverse effects of the
sympathetic nervous system. They relax blood vessels, lower blood pressure, decrease
afterload, and decrease cardiac workload. Betablockers, such as carvedilol (Coreg),
bisoprolol (Zebeta) and sustainedrelease metoprolol (Toprol XL), have been found to
improve functional status and reduce mortality and morbidity in patients with HF (Burchum &
Rosenthal, 2016). In addition, beta-blockers have been recommended for patients with
asymptomatic systolic dysfunction, such as those with a decreased EF, to prevent the onset
of symptoms of HF. The therapeutic effects of these drugs may not be seen for several
weeks or even months. Beta-blockers may produce a number of side effects, including
dizziness, hypotension, bradycardia, fatigue, and depression. Side effects are most common
in the initial few weeks of treatment. Because of the potential for side effects, beta-blockers
are started at a low dose. The dose is titrated up slowly (every few weeks), with close
monitoring after each dosage increase. Nurses educate patients about potential symptoms
during the early phase of treatment and stress that adjustment to the drug may take several
weeks. Nurses must also provide support to patients going through this symptom-provoking
phase of treatment. Because betablockade can cause bronchiole constriction, these drugs
are used with caution in patients with a history of bronchospastic diseases such as
uncontrolled asthma.

Diuretics. Diuretics are prescribed to remove excess extracellular fluid by increasing

the rate of urine produced in patients with signs and symptoms of fluid overload. HF
guidelines advocate using the smallest dose of diuretic necessary to control fluid volume
(Yancy et al., 2013). Loop, thiazide, and aldosterone blocking diuretics may be prescribed
for patients with HF. These medications differ in their site of action in the kidney and their
effects on renal electrolyte excretion and reabsorption. Loop diuretics, such as furosemide
(Lasix), inhibit sodium and chloride reabsorption mainly in the ascending loop of Henle. HF
patients with severe volume overload are generally treated with a loop diuretic first (Burcham
& Rosenthal, 2016). Thiazide diuretics, such as metolazone (Zaroxolyn), inhibit sodium and
chloride reabsorption in the early distal tubules. Both of these classes of diuretics increase
potassium excretion; therefore, patients treated with these medications must have their
serum potassium levels closely monitored. Diuretics can also lead to orthostatic hypotension
and kidney injury (Pinkerman et al., 2013). Both a loop and a thiazide diuretic may be used
in patients with severe HF who are unresponsive to a single diuretic. The need for diuretics
can be decreased if the patient avoids excessive fluid intake (e.g., more than 2 qt/day) and
adheres to a low-sodium diet (e.g., no more than 2 g/day). Aldosterone antagonists such as
spironolactone (Aldactone) are potassium-sparing diuretics that block the effects of
aldosterone in the distal tubule and collecting duct. They can effectively reduce mortality and
morbidity in patients with moderate to severe HF (Pinkerman, et al., 2013). Serum creatinine
and potassium levels are monitored frequently (e.g., within the first week and then every 4
weeks) when spironolactone is first given. These drugs are not prescribed for patients with
an elevated serum creatinine. The type and dose of diuretic prescribed depend on clinical
signs and symptoms and renal function. Careful patient monitoring and dose adjustments
are necessary to balance the effectiveness of these medications with the side effects (see
Chart 29-2). Loop diuretics are administered IV for exacerbations of HF when rapid diuresis
is necessary. Diuretics improve the patient’s symptoms, provided that renal function is
adequate. As HF progresses, cardiorenal syndrome may develop or worsen. Patients with
this syndrome are resistant to diuretics and may require other interventions to deal with
congestive signs and symptoms.

Digitalis. For many years, digitalis (digoxin) was considered an essential agent for the
treatment of HF, but with the advent of new medications, it is not prescribed as often.
Digoxin increases the force of myocardial contraction and slows conduction through the
atrioventricular node. It improves contractility, increasing left ventricular output. Although the
use of digoxin does not result in decreased mortality rates among patients with HF, it can be
effective in decreasing the symptoms of systolic HF and may help prevent hospitalization
(Pinkerman et al., 2013). Patients with renal dysfunction and older patients should receive
smaller doses of digoxin, as it is excreted through the kidneys. A key concern associated
with digoxin therapy is digitalis toxicity. Clinical manifestations of toxicity include anorexia,
nausea, visual disturbances, confusion, and bradycardia. The serum potassium level is
monitored because the effect of digoxin is enhanced in the presence of hypokalemia and
digoxin toxicity may occur. A serum digoxin level is obtained if the patient’s renal function
changes or there are symptoms of toxicity.
 Intravenous Infusions. IV inotropes (milrinone [Primacor], dobutamine [Dobutrex])
increase the force of myocardial contraction; as such, they may be indicated for hospitalized
patients with acute decompensated HF. These agents are used for patients who do not
respond to routine pharmacologic therapy and are reserved for patients with severe
ventricular dysfunction. They are used with caution, as some studies have associated their
use with increased mortality (Ciuksza, Hebert, & Sokos, 2014). IV vasodilators such as
nitroprusside (Nipride), nitroglycerin, or nesiritide (Natrecor) may also be used in patients
with severe decompensated HF (Pinkerman et al., 2013). Patients usually require admission
to the intensive care unit (ICU) and may also have hemodynamic monitoring with a
pulmonary artery catheter or alternative technology (see Chapter 25). Hemodynamic data
are used to assess cardiac function and volume status and to guide therapy with inotropes,
vasodilators, and diuretics (Urden, Stacy, & Lough, 2014). Patients with end-stage HF who
cannot be weaned from IV inotropes may be candidates for continuous therapy at home
(Ciuksza et al., 2014).

Milrinone Milrinone is a phosphodiesterase inhibitor that leads to an increase in

intracellular calcium within myocardial cells, increasing their contractility (O’Donovan, 2013).
This agent also promotes vasodilation, resulting in decreased preload and afterload and
reduced cardiac workload. Milrinone is administered IV to patients with severe HF, including
patients who are waiting for heart transplantation. Because the drug causes vasodilation, the
patient’s blood pressure is monitored prior to administration; if the patient is hypovolemic, the
blood pressure could drop quickly. The major side effects are hypotension and increased
ventricular dysrhythmias. Blood pressure and ECG are monitored closely during and
following infusions of milrinone.

Dobutamine Dobutamine is another IV medication given to patients with significant

left ventricular dysfunction and hypoperfusion. A catecholamine, dobutamine stimulates the
beta-1 adrenergic receptors. Its major action is to increase cardiac contractility and renal
perfusion to enhance urine output. However, it also increases the heart rate and can
precipitate ectopic beats and tachydysrhythmias

Medications for Diastolic Dysfunction. Patients with predominant diastolic HF and

preserved left ventricular EF are treated differently than patients with systolic HF.
Contributing causes such as hypertension and ischemic heart disease are evaluated and
treated. These patients do not tolerate tachycardia, because it does not allow time for
ventricular filling. Beta-blockers may be used to control tachycardia from atrial fibrillation or
other causes (Pinkerman et al., 2013).

Other Medications for Heart Failure Anticoagulants may be prescribed, especially if

the patient has a history of atrial fibrillation or a thromboembolic event. Antiarrhythmic drugs
such as amiodarone (Cordarone) may be prescribed for patients with dysrhythmias, along
with evaluation for device therapy with an implantable cardioverter defibrillator (ICD) (see
Chapter 26). Medications that manage hyperlipidemia (e.g., statins) are also routinely
prescribed. Nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen (Motrin)
should be avoided because they decrease renal perfusion, especially in older adults.

Nutritional Therapy. Following a low-sodium (no more than 2 g/day) diet and avoiding
excessive fluid intake are usually recommended, although studies differ regarding the
effectiveness of sodium restriction (Yancy et al., 2013). Decreasing dietary sodium reduces
fluid retention and the symptoms of peripheral and pulmonary congestion. The purpose of
sodium restriction is to decrease the amount of circulating blood volume, which decreases
myocardial work. A balance needs to be achieved between the patient’s ability to comply
with the diet and the recommended dietary restriction. Any change in diet should consider
good nutrition as well as the patient’s likes, dislikes, and cultural food patterns. Patient
adherence is important because dietary indiscretions may result in severe exacerbations of
HF requiring hospitalization (Chung, Lennie, Mudd-Martin, et al., 2015). However, behavioral
changes in this area are difficult for many patients (see Chart 29-3).

Supplemental Oxygen. Oxygen therapy may become necessary as HF progresses.

The need is based on the degree of pulmonary congestion and resulting hypoxia. Some
patients require supplemental oxygen only during periods of activity.

Other Interventions. A number of procedures and surgical approaches may benefit

patients with HF. If the patient has underlying coronary artery disease, coronary artery
revascularization with PCI or coronary artery bypass surgery (see Chapter 27) may be
considered. Ventricular function may improve in some patients when coronary flow is
increased. Patients with HF are at high risk for dysrhythmias, and sudden cardiac death is
common among patients with advanced HF. In patients with severe left ventricular
dysfunction and the possibility of life-threatening dysrhythmias, placement of an ICD can
prevent sudden cardiac death and extend survival (see Chapter 26). Candidates for an ICD
include those with an EF less than 35% and with NYHA functional class II or III, including
those with and without a history of ventricular dysrhythmias (Yancy et al., 2013). Patients
with HF who do not improve with standard therapy may benefit from cardiac
resynchronization therapy (CRT). CRT involves the use of a biventricular pacemaker to treat
electrical conduction defects. A prolonged QRS duration on ECG indicates left bundle
branch block, which is a type of delayed conduction that is frequently seen in patients with
HF. This problem results in dyssynchronous conduction and contraction of the right and left
ventricles, which can further decrease EF (Yancy et al., 2013). (See Chapter 26 for
discussion of dysrhythmias.) The use of a pacing device with leads placed in the right atrium,
right ventricle, and left ventricular cardiac vein can synchronize the contractions of the right
and left ventricles (see Fig. 29-3). This intervention improves CO, optimizes myocardial
energy consumption, reduces mitral regurgitation, and slows the ventricular remodeling
process. For selected patients, CRT results in fewer symptoms, increased functional status,
fewer hospitalizations, and longer survival (Manne, Rickard, Varma, et al., 2013).
Combination devices are available for patients who require CRT and an ICD. See Chapter
26 for further discussion of care of patients with pacemakers and ICDs. Ultrafiltration is an
alternative intervention for patients with severe fluid overload. It is reserved for patients with
advanced HF who are resistant to diuretic therapy (Yancy et al., 2013). A dual-lumen central
IV catheter is placed, and the patient’s blood is circulated through a small bedside filtration
machine. Liters of excess fluid and plasma are removed slowly from the patient’s
intravascular circulating volume over a number of hours. The patient’s output of filtration
fluid, blood pressure, and hemoglobin (analyzed for hemoconcentration) are monitored as
indicators of volume status. Research continues regarding the effectiveness of ultrafiltration.
For some patients with end-stage HF, cardiac transplantation is one of the few options for
long-term survival. Patients with ACC/AHA stage D HF who may be eligible are referred for
consideration of transplantation. Some of these patients require mechanical circulatory
assistance with an implanted ventricular assist device as a bridge therapy to cardiac
transplantation. A left ventricular assist device may also be implanted as destination therapy
(permanent therapy) for selected patients.